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安罗替尼联合培美曲塞对晚期非鳞非小细胞肺癌jak/STAT3信号传导通路的影响

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实用癌症杂志 2024年第6期39卷 981-983,987页

作者：郑庆凯程文静郑红陈苗赵晓光河南省焦作市人民医院 454000

目的研究安罗替尼联合培美曲塞对晚期非鳞非小细胞肺癌jak/STAT3信号传导通路的影响。方法选取82例晚期非鳞非小细胞肺癌患者为此次试验对象,随机分成2组。对照组(41例)术后接受培美曲塞治疗,实验组(41例)在此基础上联合安罗替尼治疗。... 详细信息

目的研究安罗替尼联合培美曲塞对晚期非鳞非小细胞肺癌jak/STAT3信号传导通路的影响。方法选取82例晚期非鳞非小细胞肺癌患者为此次试验对象,随机分成2组。对照组(41例)术后接受培美曲塞治疗,实验组(41例)在此基础上联合安罗替尼治疗。对比两组患者治疗前后Janus激酶(jak)、转录激活因子3(STAT3)表达情况;对比两组患者临床疗效和化疗不良反应。结果治疗后两组患者jak、STAT3表达均明显降低,且相比于对照组,实验组显著更低(P0.05)。结论对于晚期非鳞非小细胞肺癌患者,在培美曲塞基础上联合安罗替尼治疗,可有效抑制jak/STAT3信号传导通路活性,临床疗效较高,并且不会增加不良反应的发生。

关键词：安罗替尼培美曲塞肺癌 jak STAT3

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系统性红斑狼疮诊疗有了新思路 001

系统性红斑狼疮诊疗有了新思路

美国Palmetto State武器公司jakL步枪

中国科学报

作者：江庆龄

本报讯（见习记者江庆龄）上海交通大学医学院附属仁济医院风湿科教授沈南和中-澳个体化免疫学联合研究中心教授卡罗拉·维努埃萨团队，在国际上首次揭示了转录因子ZEB2对狼疮致病性B细胞新亚群ABC细胞谱系特化的调控功能和机制。相关... 详细信息

本报讯（见习记者江庆龄）上海交通大学医学院附属仁济医院风湿科教授沈南和中-澳个体化免疫学联合研究中心教授卡罗拉·维努埃萨团队，在国际上首次揭示了转录因子ZEB2对狼疮致病性B细胞新亚群ABC细胞谱系特化的调控功能和机制。相关研究近日发表于《科学》。系统性红斑狼疮

关键词：系统性红斑狼疮自身免疫疾病 jak

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轻兵器 2024年第6期 1-1页

美国Palmetto State武器公司成立于2008年,位于美国南卡罗莱纳州,该公司名称即来自于南卡罗莱纳州绰号“棕榈之州”(The Palmetto State)。公司最初以生产AR-15系步枪起家,后来开始生产AK系步枪,2019年公司与FN美国分公司开展合作。jak... 详细信息

美国Palmetto State武器公司成立于2008年,位于美国南卡罗莱纳州,该公司名称即来自于南卡罗莱纳州绰号“棕榈之州”(The Palmetto State)。公司最初以生产AR-15系步枪起家,后来开始生产AK系步枪,2019年公司与FN美国分公司开展合作。jakL步枪即是在FNSCAR步枪基础上改进的民用步枪,被称为Palmetto State版SCAR步枪。该枪基本结构与SCAR相同,仍采用一体式机厘/护手结构,不同之处是其护手改为上、下结构,上、下护手通过两侧各2个螺钉固定在一起。上护手顶部设有与机匣顶部一体式的皮卡汀尼导轨,下护手左右两侧及底部均设有M-Lok导轨接口。

关键词： jak 一体式 CAR

Efficacy and safety of jak inhibitor INC424 in patients with primary and post-polycythemia vera or post-essential thrombocythemia myelofibrosis in the Chinese population

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Frontiers of Medicine 2016年第4期10卷 437-443页

作者： Xin Du Daobin Zhou Department of Hematology Guangdong General Hospital Guangdong Academy of Medical Sciences Cruangzhou 510080 China Department of Hematology Peking Union Medical College Hospital Beijing 100730 China

A phase II study （A2202） was performed to evaluate the efficacy and safety of jak inhibitor ruxolitinib in 63 Chinese MF patients. Ruxolitinib was given twice a day （bid） at a starting dose of 15 mg （n = 25） or 20 mg （n = 38） based on a baseline platelet count. About 94.7% of the patients achieved a reduction in spleen size, 27.0% of which exhibited significant reduction （≥35%） at week 24. Significant improvement in debilitating constitutional symptoms, as assessed by MFSAF v2.0, was observed in patients treated with ruxolitinib. Ruxolitinib treatment was generally weli tolerated by Chinese patients. Although the treatment was associated with an increase in certain adverse events （AEs） that were established as identified risks （anemia and thrombocytopenia）, these AEs were considered manageable in this clinical setting. Ruxolitinib provided substantial reductions in splenomegaly and improvements in symptoms, and was well-tolerated by Chinese patients with MF.

关键词： jak ruxolitinib Chinese patients myelofibrosis

Overexpression of jak1 Activating Mutants in Hepatocytes Is Insufficient to Generate Hepatocellular Carcinoma in Zebrafish

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Journal of Genetics and Genomics 2016年第2期43卷 99-102页

作者： Yue Yuan Jian Zhang Qin Zhou The Division of Molecular Nephrology and the Creative Training Center for Undergraduates the M.O.E.Key Laboratory of Laboratory Medical Diagnosticsthe College of Laboratory MedicineChongqing Medical UniversityChongqing 400016China State Key Laboratory of Developmental Biology Institute of Genetics and Developmental BiologyChinese Academy of SciencesBeijing 100101China

Hepatocellular carcinoma （HCC）, a major subtype of liver cancers, is a prevalent human malignancy worldwide. In men, HCC is the fifth frequently diagnosed cancer but the second most common cause of cancer death. In women, it ranks seventh in cancer diagnosis and sixth in cancer-related death （Jemal et al., 2011）. Unlike some other cancers, such as breast cancer and colon cancer, the molecular etiology of HCC re- mains largely unknown. Infection of hepatitis virus is considered as a major risk factor in the development of liver cancers （Parkin, 2006）. Currently, there are limited options to treat HCC except for chemotherapy. Elucidating molecular mechanism of hepatocyte transformation will help develop new treatments for cancer. The widely accepted multi-step progression of carcinogenesis consists of genetic alterations which regulate cell proliferation, apoptosis and so on （Vogelstein and Kinzler, 1993）. Moreover, abnormal activation of signaling pathways has been proposed as an oncogenic driver for cancer development. For example, Kras activation occurs in 7% of human liver cancer patients. Activated Kras is sufficient to induce robust liver tumorigenesis in transgenic animal models （Nguyen et al., 2011）.

关键词： cell HCC Overexpression of jak1 Activating Mutants in Hepatocytes Is Insufficient to Generate Hepatocellular Carcinoma in Zebrafish jak

Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injury

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Neural Regeneration Research 2015年第9期10卷 1390-1392页

作者： Pere Boadas-Vaello Enrique Verdú Research Group of Clinical Anatomy Embryology and Neuroscience (NEOMA) Universitat de Girona Faculty of Medicine Department of Medical Sciences

Traumatic spinal cord injury （SCI） causes motor paralysis, sensory anesthesia and autonomic dysfunction below the le- sion site and additionally some SCI patients refer neuropathic pain together with these signs and symptoms. Clinical and experimental studies have revealed the main pathological changes of injured spinal cord implicated in all these signs and symptoms, including neuropathic pain. After few hours of traumatic SCI, it is usual to observe broken blood brain barrier with plasma and blood cells extravasation, cell necrosis, disruption of ascending and descending spinal cord pathways and increased potassium and glutamate. Glutamate contributes to excitotoxicity of neurons whereas potassium facilitates ectopic depolarization of survival neurons and activation of resident microglia.

关键词： EGCG jak STAT NF Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injury SCI

Effects of Inhibiting jak on Invasion and Metastasis of the Human Breast Cancer Cells through ERK Signaling Transduction Pathway

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Chinese Journal of Cancer Research 2009年第1期21卷 32-36页

作者： Jing Zhao Hong-fang Chen Hua-yu Deng Department of Pathophysiology Chongqing Medical University Chonging 400016 China

Objective： To explore the effects of Janus activated kinase （jak） inhibitor AG490 on the phosphorylation of extracellular signal regulated protein kinase （ERK） in human breast cancer cells MDA-MB-231 and the roles of jak in the invasion and metastasis of the human breast cancer cells through ERK signaling transduction pathways. Methods： MDA-MB-231 cells were treated with 20 μmol/L, 40 μmol/L, 80 μmol/L Janus kinase inhibitor AG490 for 24, 48 and 72 h. Proliferation and adhesion of MDA-MB-231 cells to matrigel were measured with MTT assay. When treated with 40 μmol/L AG490 for 24 h, the expressions of P-ERK and MMP-9 of cells were detected by Western-blot and invasion and metastasis of MDA-MB-231 cells were evaluated with transwell chamber. Results： After being treated with 20 μmol/L, 40 μ/L, 80 μmol/L AG490 for 24, 48 and 72 h, the proliferation of MDA-MB-231 cells was inhibited in a dose-and time-dependent manner. MDA-MB-231 cells treated with 40 μmol/L AG490 for 30, 60, 90 and 120 rain resulted in the increasing adhesion of cells to Matrigel in a time-dependent manner. However, capacity of adhesion in the group treated with AG490 was significantly decreased in comparison with the control group （P〈0.01）. The expression level of P-ERK and MMP-9 were decreased when treated with AG490. After treatment with 40 μmol/L AG490, in invasion assay, the number of cells in AG490 treated group to migrate to filter coated with Matrigel was reduced compared with control group （P〈0.05） Meanwhile, in migration assay, the number of cells in AG490 treated group to migrate to filter was also decreased compared with control group （P〈0.05）. Conclusion： Our study indicates that jak kinase could affect the activity of ERK signal transduction pathway through the phosphorylation of ERK. The inhibitory effects of jak kinase on MMP-9 expression and invasion of breast cancer cells were associated with the down-regulation of the ERK signaling pathway.

关键词： Breast cancer jak ERK Invasion Metastasis

Interleukin-6 role in head and neck squamous cell carcinoma progression

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World Journal of Otorhinolaryngology-Head and Neck Surgery 2016年第2期2卷 -页

作者： Moaz M. Choudhary Thomas J. France Theodoros N. Teknos Pawan Kumar Department of 0tolaryngology-Head and Neck Surgery and Comprehensive Cancer Center The 0hio State University Columbus 0H 43210 USA

Interleukin-6 (IL-6) is a pleiotropic cytokine which plays an important role in a number of cellular processes including proliferation, survival, differentiation, migration and invasion. IL-6 mediates its downstream effects by activating a number of signaling cascades including jak/STAT, PI3K/AKT and MAPK pathways. In addition to its effects on tumor cells, IL-6 also regulates tumor progression and tumor metastasis by modulating tumor angiogenesis and tumor lymphangiogenesis. A number of studies have shown that IL-6 levels are markedly upregulated in cancer patients. We and others have shown that high IL-6 expression independently predicts tumor recurrence, tumor metastasis and poor survival in head and neck cancer patients. Therefore targeting IL-6 signaling is a potential therapeutic strategy for the treatment of head and neck squamous cell carcinoma (HNSCC). In this review, we discuss the current understanding of the role of IL-6 in HNSCC progression and potential therapeutic strategies to target IL-6 signaling for the treatment of head and neck cancer patients.

关键词： Head and neck squamous cell carcinoma Interleukin-6 jak MAPK Nanog PI3K/Akt STAT3

祛风明目丸对EAU大鼠jak/STAT通路关键蛋白表达的影响

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祛风明目丸对EAU大鼠JAK/STAT通路关键蛋白表达的影响

作者：张诚颖湖南中医药大学

学位级别：硕士

目的:观察祛风明目丸对实验性自身免疫性葡萄膜炎(Experimental autoimmune uveitis,EAU)大鼠眼前节炎症反应及组织病理学表现,评估祛风明目丸对EAU大鼠的疗效,以及对EAU大鼠视网膜组织中jak/STAT通路关键蛋白表达的影响,探讨祛风明目丸... 详细信息

目的:观察祛风明目丸对实验性自身免疫性葡萄膜炎(Experimental autoimmune uveitis,EAU)大鼠眼前节炎症反应及组织病理学表现,评估祛风明目丸对EAU大鼠的疗效,以及对EAU大鼠视网膜组织中jak/STAT通路关键蛋白表达的影响,探讨祛风明目丸在EAU大鼠中的可能作用机制。方法:将70只SPF级雄性Lewis大鼠(140眼)根据随机数字表法随机选取19只为空白组,剩余为造模组进行主动免疫,即在后腿内侧通过皮下注入含视网膜光感受器间维生素A类结合蛋白(inter-photoreceptorretinoid binding protein,IRBP)的弗氏完全佐剂(Completefreund's adjuvant,CFA)乳糜液的方法,对Lewis大鼠进行主动免疫,连续4天,建立EAU大鼠模型。自免疫后第1天,观察大鼠眼前节炎症表现,参照炎症分级进行评分,造模成功的EAU大鼠按随机数字表法分为模型对照组、祛风明目丸低剂量组、祛风明目丸正常剂量组(以下简称对照组、低剂量组、正常剂量组),每组16只。每组大鼠按计划进行给药处理。分别于造模后第7天及灌胃后第14天取相应大鼠眼球视网膜组织进行HE染色制作病理切片,进行组织病理学检查。采用免疫印迹(Western Blot)检测方法检测大鼠视网膜组织中jak、STAT1、STAT3蛋白相对表达量。结果:1.组织病理学结果显示,免疫后第7天,模型组组织切片病理评分高于空白组,EAU大鼠模型成功建立。给药后第14天,祛风明目丸干预组视网膜组织结构破坏程度明显轻于模型组,表明药物干预发生作用。2.Wb检测结果显示,与空白对照组比较,模型对照组jak、STAT1、STAT3均呈高表达,结果具有统计学意义(Pjak、STAT1、STAT3均呈低表达,结果具有统计学意义(Pjak、STAT1、STAT3的表达,说明jak、STAT1、STAT3可能是祛风明目丸作用于EAU大鼠的靶点,即可通过抑制以上靶点达到改善EAU病理过程的目的。2.祛风明目丸可能通过抑制致葡萄膜炎性的jak/STAT信号通路中jak、STAT1、STAT3蛋白的表达发挥其抗炎作用。

关键词： EAU大鼠祛风明目丸 jak STAT1 STAT3